Archive for the ‘Hypothyroidism’ Category

Understanding Thyroid Disease

Although thyroid disease/disorders do not cause HE, virtually all HE patients are eventually diagnosed with Hashimoto’s Thyroiditis – an autoimmune disease that attacks the thyroid gland.  There are some excellent places on the web to find information about the thyroid gland, thyroid disorders, and treatment.  Here are some  recommended  websites with scientific information, articles, and case studies:  (to read the most current issue of their journal, click here: )

Treating the Thyroid with “Normal” TSH Levels

February 24, 2010 2 comments

How much of HE is related to thyroid dysfunction?  Will treating a patient with “normal” thyroid hormone levels help with the HE symptoms?  How much of all this is related?  We really don’t know.

This post addresses the link between Levothyroxine, used to treat hypothyroidism, and its benefit on HE.

Mary Shomon, well known thyroid patient advocate, wrote an article “Do You Need Preventative Thyroid Treatment: Treating Antibodies When TSH is Normal“.  A lot of us HE patients fall into the category of having high anti-TPO antibodies but “normal” TSH, T3 and T4 thyroid levels.  A lot of us later develop hypothyroid symptoms, then it takes even longer to be diagnosed with hypothyroidism and finally receive treatment.

Recent studies show, preventative treatment could slow or even stop the development of hypothyroidism, and reduce the antibodies.  However, at this point, most endocrinologists will dismiss you if you talk about preventative treatment.  I have been dismissed many times by many endos, and now have developed almost all of the classic symptoms of hypothyroidism.  This possibly could have been prevented.

She notes a recent study (that I currently can’t find a link to):

En-Ting Chang, Du-An Wu, Dee Pei, Shi-Wen Kuo, Ming-Chen Hsieh. [P2-552] Influence of L-Thyroxine Administration in Patients with Euthyroid Hashimoto’s Thyroiditis. Endocrine Society Endo 2005 Abstracts

In this study on HT patients with normal range TSH, but high antibodies, half were given levothyroxine and half were not treated.  “Those receiving levothyroxine had substantially decreased auto-antibody levels; levels actually increased in some among the untreated group. TSH levels also decreased in the treated group, averaging 0.5 vs 2.5 in the untreated group. The researchers concluded that early prophylactic (preventative) levothyroxine treatment might be useful to help slow down the progression of the autoimmunity of Hashimoto’s Thyroiditis.”

Euthyroidism (patients having normal TSH levels):

In the study “One-Year Prophylactic Treatment of Euthyroid Hashimoto’s Thyroiditis Patients with Levothyroxine: Is There a Benefit?“, euthyroid HT patients were given levothyroxine as a prophylactic to see if it would benefit the autoimmune process.  Half of the patients were treated with levothyroxine, the other half were not treated.  The study states, “After 1 year of therapy with LT4, TPO-Abs and B lymphocytes decreased significantly only in the treated group of euthyroid patients with HT (p < 0.05). In contrast, TPO-Abs levels did not change or even increased in untreated euthyroid patients with HT.”

The study also states, “Prophylactic treatment of euthyroid patients with HT reduced both serological and cellular markers of autoimmune thyroiditis. Therefore, prophylactic LT4 treatment might be useful to stop the progression or even manifestation of the disease.”

The purpose of the 2008 study, “Long-Term Follow-Up of Antithyroid Peroxidase Antibodies in Patients with Chronic Autoimmune Thyroiditis (Hashimoto’s Thyroiditis) Treated with Levothyroxine” was to see if patients treated with levothyroxine for HT reached the point where their TPO-Ab levels became within normal range (negative).

In the study, 92% of patients had a decrease in their TPO-Ab levels.  “The mean decrease after 3 months was 8%, and after 1 year it was 45%. Five years after the first value, TPO-Ab levels were 1456 ± 1219 IU/mL, a decrease of 70%. TPO-Ab levels became negative, < 100 IU/mL, in only six patients, a normalization percentage of 16%.”

The conclusion of the study was “Serum TPO-Ab levels decline in most patients with Hashimoto’s thyroiditis who are taking levothyroxine, but after a mean of 50 months, TPO-Ab became negative in only a minority of patients.”

The aim of the 2008 study “Effects of Prophylactic Thyroid Hormone Replacement in Euthyroid Hashimoto’s Thyroiditis” was “to evaluate the effects of prophylactic L-thyroxine treatment on clinical and laboratory findings of patients who were euthyroid at the time of diagnosis.”  The study states, “After 15 months of L-thyroxine treatment, there was a significant increase in free T4 and a significant decrease in TSH and anti-thyroglobulin antibody anti-thyroid peroxidase antibody levels.”  “In conclusion, prophylactic thyroid hormone therapy can be used in patients with Hashimoto’s thyroiditis even if they are euthyroid.”

The study goes on to conclude, “Early treatment of Hashimoto’s Thyroiditis with L-thyroxine may slow down not only the disease process itself but through its immune modulating events it may also affect the course of other autoimmune diseases which accompany.”

This would relate to HE and the HE patient would benefit from the lowering of the antibodies as well, with less side effects from levothyroxine than steroids. 

Subclinical Hypothyroidism (borderline levels):

A 2008 study, “Diagnostic strategies for subclinical hypothyroidism” notes “45 of the 61 subclinical hypothyroid patients had elevated anti-TPO levels (73%). This is an important finding suggesting an autoimmune etiology for subclinical thyroid dysfunction with a higher risk of developing overt hypothyroidism.”  This study states that the antibodies should be considered in order to treat subclinical hypothyroidism.

A 2006 study “Subclinical Hypothyroidism“, notes “the titer of anti-thyroid peroxidase (TPO) antibodies is proportional to the degree of lymphocytic infiltration and inflammation within the gland. Thus, hypothyroidism in patients with high titers of anti-TPO antibodies is more likely to progress from subclinical to overt disease.”   “Without treatment, progression to overt hypothyroidism is likely”.  He also states, “Endocrinologists also disagree about the normal range for serum TSH levels. Although many laboratories have traditionally used 4 to 6 mIU/L as the upper limit of normal, the data used to calculate reference ranges have frequently included measurements in patients who had positive results on anti-TPO antibody tests or other evidence of early thyroid dysfunction. Careful analysis suggests that the true upper limit of normal for serum TSH concentration is closer to 2.5 mIU/L.”

Spontaneous Remission or Levothyroxine?

One patient in the case study “An 85-year-old Case with Hashimoto’s Encephalopathy, Showing Spontaneous Complete Remission” was taking thyroxine treatment at the time of his remission.

The case study, “Long-Term Treatment of Hashimoto’s Encephalopathy” states “35% of cases had subclinical hypothyroidism; 22% were euthyroid not on levothyroxine; 20% had overt hypothyroidism; and 8% were euthyroid on levothyroxine (as were our two cases); 7% had hyperthyroidism (5% overt, 2% subclinical); 6% had unknown thyroid status; and 1% did not have thyroid disease. A goiter was present in 62% of cases (see Table 2). Of the above cases with subclinical or overt hypothyroidism, 17% improved following treatment with levothyroxine alone, while 40% improved following combined treatment with levothyroxine and steroids.2 It is somewhat surprising that some cases improved with levothyroxine treatment alone. However, it may be that those cases were destined to improve spontaneously.

The study summarized the treatment efficacy of reviewed literature, reporting “improvement in 98% of cases treated with steroids, 92% treated with steroids and levothyroxine, and 67% treated with levothyroxine, while 9% of cases did not improve with any of the above combinations.”

The study notes that it is interesting that some cases responded with levothyroxine treatment alone, and they hypothesize that these patients may have been destined to improve spontaneously.  Perhaps the levothyroxine reduced the antibody levels enough to improve the HE symptoms.  After all, we still don’t know the exact pathology of the link between the antibodies and the encephalopathy.  But we do know there is a link.

My ending thoughts on this post:

Considering most HE patients eventually develop hypothyroidism, those with hypothyroid symptoms (regardless of the “normal” level of their TSH) should be treated with levothyroxine and monitored regularly for further thyroid problems.  The side effects of levothyroxine are minimal and it has been shown to improve HE symptoms in some case studies, even leading to remission. 

Rather than just steroids, perhaps a combination of steroids and levothyroxine should be considered as a primary treatment for HE.